NK6 Homeobox 2 Regulated Gastrokin-2 Suppresses Gastric Cancer Cell Proliferation and Invasion via Akt Signaling Pathway
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ORIGINAL PAPER
NK6 Homeobox 2 Regulated Gastrokin-2 Suppresses Gastric Cancer Cell Proliferation and Invasion via Akt Signaling Pathway Jin Dai1 Tieli Peng1 Xiangdi Yu ●
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Accepted: 22 September 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract This study aims to explore the role of Gastrokin-2 (GKN2) in gastric cancer and its function in the progression and metastasis of gastric cancer. The expression of GKN2 in the patient samples was examined by qRT-PCR and western blot. The transcription factor NK6 Homeobox 2 (NKX6-2), which binds to the GKN2 promoter, was predicted by cBioportal and JSPAR. Binding between NKX6-2 and the GKN2 promoter was analyzed by dual-luciferase assay. MTT assay and transwell assay were used to detect changes in gastric cancer cell viability and migration after GKN2 overexpression, which was achieved by transfection of GKN2 overexpression vector. Akt signaling pathway markers were assessed by western blot. GKN2 is downregulated in gastric cancer and low GKN2 expression is correlated to poor survival, metastasis, and higher clinical stages. NKX6-2 binds the promoter region of GKN2 and regulate its expression. GKN2 overexpression inhibits the proliferation, migration, and invasion of gastric cancer cells, which was mediated by Akt signaling pathway. NKX6-2 regulated GKN2 inhibits the proliferation and invasion of gastric cancer cells by inhibiting Akt signaling pathway. GKN2 can be used as a potential diagnostic and therapeutic target for patients with clinical gastric cancer. Keywords NKX6-2 Gastric cancer Akt signaling pathway GKN2 ●
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Abbreviations Gastrokin-2 GKN2 NKX6-2 NK6 Homeobox 2 EMT epithelial-mesenchymal transition FBS fetal bovine serum TCGA the Cancer Genome Atlas STAD Stomach Adenocarcinoma MTT 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide SD standard deviation
* Xiangdi Yu [email protected] 1
Department of Gastroenterology, Qingyuan People’s Hospital, the Sixth Affiliated Hospital of Guangzhou Medical University; Institute of Digestive Disease of Guangzhou Medical University, Guangzhou 511518 Guangdong, China
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Department of Anesthesiology, Guizhou Provincial People’s Hospital, Guiyang 550003 Guizhou, China
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Introduction Gastric cancer is one of the most common high-risk, highmortality malignant tumors worldwide [1, 2]. Because of the difficulty in the early diagnosis of gastric cancer, most gastric cancer patients have advanced-stage cancers, and are not eligible for curative resection. The main cause of death in patients with advanced gastric cancers is tumor metastasis, i.e. the spread of cancer cells in secondary organs [3, 4]. Therefore, there is an urgent need to elucidate the mechanism of gastric cancer metastasis and develop strategies to impede cancer metastasis. Epithelial-mesenchymal transition (EMT), which refers to the decrease of polarity and intercellular adhesion by epithelial cells and transitioning to cells with high motility in tumor stroma, is a driving force o
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